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>>CHEST BY
NUMBERS
1.
Chest
measurements
a.
Carina at T4-5; normal carina angle 60-100deg
b.
Interlobar artery <16mm
c.
MPA <3cm
d.
Left hila 1-2cm higher than highest point of
right hila
e.
R paratracheal stripe ≤5mm
f.
Vascular pedicle= 38-58mm (should be <7cm
otherwise widened mediastinum) on PA view (measure near level azygous
vein; from
where SVC meets RMSB and to where a perpendicular line is drawn from
left
subclavian exiting Ao arch)
g.
Azygous trans dia <1cm upright and
<1.5cm supine
h.
Kids humeral head ossific center at >37wks
(term); femoral head ossific center at 4mos
i.
Kids normal 6ribs ant and 8ribs post (hypeinflation 8ribs
ant/10ribs post;
hypoinflation 4ribs post)
j.
Normal thymus (homogenous, bilobed/triangular
with concave lateral margins on CT; size increases from birth to age
8yo then
decreases; 18mm thickness <20yo and 13mm in older pts; rebound
thymic
hyperplasia if volume increases by 50%)—sail sign (right) or wave sign
(smooth
indentations)
k.
Thoracic aorta (ectasia 3.7-4.0cm, mild
enlargement 4.0-4.5cm, ≥4.5cm aneurysm, ≥6cm surgery)
i.
LVOT
ii.
Aortic annulus (at valve)
iii.
Aortic root (SOV)
1.
“Cusp to cusp”
measurement (cardiologists) upto 4cm
2.
Mean “cusp to
commisure” (preferred)
iv.
Sinotubular jct (STJ)
v.
Asc aorta (@MPA) upto 3.7cm
vi.
Aortic arch
vii.
Aortic isthmus (btwn take off of left
subclavian
artery and ductus arteriosus)
viii.
Prox desc
aorta (@MPA)
ix.
Distal desc aorta (@dia hiatus) upto
2.8cm
l.
Normal pericardial thickness=2mm (>4mm is
concerning for pericarditis)
m.
Pericardial fluid: normal 15cc (post CPA
blunting with >75cc, lat CPA blunting with >250cc,
complete opacification
atleast 500cc); >1cm decub free-flowing eff can be tapped
without imaging
guidance
n.
Left Atrium AP <4cm
o.
Left Ventricle chamber transverse in ED
<5cm
p.
LV wall thickness <12mm
q.
Haller index of pectus excavatum (transverse
dia divided by AP diameter) normal ≤2.5 (>3.2 is one criteria
for surgical
correction)
r.
PTX >25% requires chest tube evacuation
(calculator= ww.chestx-ray.com/calculator)
s.
Normal dia excursion of 1-2ribs on fluoro
sniff test (unless there is mod to large effusion)
2.
Lines/Tubes (“correlate for preferred/desired
location/placement”)
a.
ETT=
2-6cm above carina and atleast 3cm
below vocal cords (carina is usually at about T6; vocal cords at
C6)—should be
below inf aspects of clavicles (thoracic inlet); cuff <3cm in
dia (without
bowing of tracheal walls); tube dia should be 2/3 of tracheal dia
b.
Trach tube=
should be halfway btwn neck entrance
site and carina
c.
SGC
(for pulm capillary WP)=tip should be
distal to pulmonic valve; on the right, measure from where catheter
crosses
itself and should be within 2cm (should next extend beyond proximal
interlobar
pulm artery); on the left, measure from most sup turn of catheter at
hila and
should be within 2cm
d.
Pacer/AICD
(all are pacers; AICD has sensing and
shocking electrodes for cardioversion/defibrillation)
i.
Single
lead= RV; Dual lead= RA and RV; Triple lead (biventricular for CRT)=RA,
RV, and
coronary sinus
ii.
Battery can
with lead pins; leads
iii.
Look for
broken lead (lead damage); dislodged lead tip (pulled back); Twiddler’s
syndrome
e.
IABP
(intra-aortic counterpulsion balloon
pump for cardiogenic shock)=inflates during diastole; radiopaque tip
1cm distal
to left subclavian; projecting 1-2cm below top of arch
f.
Chest tube
(pleural drain, thoracostomy tube,
pigtail cath)=tip and side ports within thoracic cavity; anterosuperior
placement for PTX; posteroinferior placement for effusion; exclude tube
within
fissure or intra-pulmonary placement
g.
NGT/OGT
(enteric tube)=tip within stomach,
distal to GEJ (side port is located 6cm from the tip); note if coiled
or
post-pyloric
h.
DHT
(feeding tube)=weighted tip should be
within 2nd or 3rd portion
of duo (prefer near distal 4th
portion of duo neat LOT)
i.
CVC
(tunneled dialysis cath, PICC, port-a-cath
(chest ort) with Huber needle access)=IJ/subclavian/femoral; tip near
superior
cavo-atrial junction or caudal aspect of SVC; should be medial to 1st
rib on frontal and caudal and posterior to clavicle (otherwise suspect
intra-arterial)
j.
UVC=
umbilicusàUVàleft PVàductus venosusàIVC; tip at or slightly above dia at
inf cavo-atrial jct; curves medially (convex laterally) thru liver on
frontal;
on lateral view, directed ant-sup then horiz-post and then heads sup
towards
heart
k.
UAC=
umbilicusàUAàinternal
iliacàcommon
iliacàaorta
(ascends parallel to spine);
normal high=T6-T9 (above dia); normal low=below L2 (more complications
if at
L1-2 level of renal arteries); dips inferiorly then ascends superiorly
parallel
to spine
l.
Epicardial leads
m.
Implantable loop recorder (for rhythm)
n.
Neurostimulator with epidural leads/electrodes
o.
ECMO
(extra-corporeal membrane
oxygenation) in kids
i.
VV
(veno-venous) vs VA (veno-arterial)
ii.
VV=Draining
large venous cannula via RIJ (make sure tip and side port within RA);
smaller
returning venous catheter via femoral vein (tip within IVC at or above
inferior
cavo-atrial jct)
iii.
VA=also
has an arterial returning cannula usually within R CCA (tip projects
over arch
at origin of innominate artery)
iv.
Normal to
have diffusely opacified lungs
p.
VAD
(ventricular assist device)—bridge to
cardiac transplant
i.
Percutaneous
vs surgically implanted
ii.
LVAD,
RVAD, BIVAD
iii.
Conduits
(inflow vs outflow), pump, driveline
iv.
Look for
kinking of cannula/conduit
v.
Percutaneous
VAD (Impella): tip within LV; outflow portion within LVOT
>>SPN
1.
Solid
nodules
a.
Size:
1-3mm=miliary; 3-5mm=micronodule;
>5mm=macronodule; >3cm=mass
b.
B9
calc= central, diffuse, laminated
(concentric), popcorn
c.
Malig
calc= eccentric, stippled, amorphous
d.
Margins=
smooth, lobulated (bad), spiculated
(bad)
e.
Attenuation=
fat (<-40HU) suggests hamartoma
f.
Location=
subpleural, juxtapleural,
perifissural, pleural-based, along mediastinal pleural surface,
peribronchovascular,
endobronchial
g.
Others=satellite
nodule suggest infx; pleural
tag (bad); central lucency (aka ABG) ddx is BAC,
lymphoma, OP
h.
Enhancement
<15HU is likely benign (>20-25HU
is probably malignant ~98% sensitive for CA)
i.
Volume
Doubling Time= increase in dia by 25%
correlates with doubling of volume (malig VDT usually btwn 30-500d)àsee
calculator on
chestxary.com
j.
DDX
solid non-calcified nodule=non-calcified
granuloma, intrapulm LN, CA
k.
DDX
airspace/macrondules nodules= acute
varicella (classic), mets, fungal, aspergillosis, kaposi
l.
DDX
calcified micronodules= fungal
(histo)/TB, alveolar microlithiasis, malig calcifications, healed
varicella,
silicosis, mets
m.
DDX
cavitating mets= primary SCC,
secondary SCC (H&N males and cervical females), sarcoma
n.
DDX
calcifying mets=
osteo/chondrosarcoma, mucinous colon, leimyosarcoma
o.
DDX
cannon-ball mets (>3cm)= MCSaR
melanoma, colon, sarcoma, RCC
p.
DDX
nodules with GG halo (hemorrhagic)=
hemorrhagic mets (chorioCA), invasive aspergillosis, kaposi, CMV
q.
DDX
mets in kids= T-ROWEN testicular,
rhabdomyosarcoma, osteosarcoma, wilms, ewings, neuroblastoma
r.
DDX
nodules in HIV= TB/fungal, CMV (GG),
Kaposi (flame-shaped), aspergillosis (GG halo), PCP (cystic UL),
lymphoma
s.
PET/CT:
size ≥8mm; low (<5%)
to mod
(5-60%) prob or CA; not for very low prob or high prob; discordance
btwn
pretest prob and imaging test; for staging
t.
PET/CT
sensitivity for BAC is 10-30% and false
neg rate for carcinoid is 25%
u.
PET/CT
overall sens 97% and spec 80% for
characterizing SPN >1cm in dia
v.
NLST
NEJM 2011 LDCT for lung CA screening
“reduced lung CA mortality by 20% with LDCT vs CXR screening
w.
High
risk pts per Fleischner society=smoker, 1st
deg relative with lung CA, exposure to asbestos/radon/uranium
x.
Fleischner
society criteria does not apply to:
age<35yo, known/suspected extra-thoracic CA, infectious symptoms
(unexplained fever), non-solid nodules
y.
Screening
chest CT criteria (ACR): 55-80yo with
30pack-yr smoking hx who is current smoker or quit 15yr ago
2.
Non-solid
nodules
a.
GGN
(pure GG nodule)
i.
Ddx=
atypical adenomatous hyperplasia (precursor to adenoCA) vs AdenoCA
(BAC) vs
infx/inflammatory vs focal fibrosis
ii.
<5mm
don’t need f/u esp if enrolled in lung nodule program; but if multiple
(then do
FU in 1yr)
iii.
≥5mm
FU in 3-6 mos à
if stable FU for total of 3-5yr vs if enlarge or
develop solid component
recc resection
b.
PSN
(part-solid nodule)
i.
FU
in 3-6mos à
if persist consider PET/CT (some say resect) vs if
enlarge recc
resection
3.
SCREENING
CHEST CT
a.
NLST
(national lung screening trial)
b.
Published
2011 in NEJM (“Reduced lung cancer
mortality with low-dose CT screening”)
c.
Pts
who received low dose CT had 20% lower risk
of dying from lung CA than those who received CXR
d.
Screening
chest CT criteria (ACR): 55-80yo with
30pack-yr smoking hx who is current smoker or quit 15yr ago
e.
What
is considered low dose CT
i.
Prefer
≥16 detector CT with gantry rotation time ≤0.5s
ii.
Slice
thickness ≤2.5mm (with recon interval ≤ slice thickness) and use ≤1mm
for MPRs
iii.
End-inspiration
iv.
Non-contrast
v.
CTDI
vol ≤3mGy for “standard” size pt (DLP ≤75mGy-cm or Est dose ≤1mSv)
f.
Reporting
i.
Use
Lung-RADs version1
ii.
Size
(measure on lung windows; give avg dia & round it to nearest
whole number)
iii.
Location
(lobe/seg)—give image#
iv.
Attenuation
(soft tissue, calcified, mixed)
v.
Opacity
(solid, part-solid, GG)
vi.
Margin
(smooth, lobulated, spiculated)
vii.
Comparison
(compare to oldest scan)—increase in size by >1.5mm is
significant
>>AIRWAYS (see HRCT for small airways dz and
bronchiolitis)
1.
Airways thickening on CXR (cheerios
and dirty lung): non-specific findings seen with reactive-airways
disease
(asthma) vs sequel of smoking vs bronchitis(clinical diagnosis)
2.
Airways lesions
a.
B9 solitary=mucus
plug, FB, papilloma (multiple
in kids; malig transformation to SCC in 10% of adults)
b.
Multiple airways lesions=papillomatosis,
mets, TBO/RP/amyloidosis, TB
c.
Malignant Trachea=”SAM” SCC,
adenoid cystic, mets (breast, melanoma)
d.
Malignant Bronchus=”BCMM” bronchogenic
tumor (SCC, small cell),
carcinoid (enhances, 1/3calcified, tip-of-iceberg), mucoepidermoid,
mets
(breast, melanoma)
3.
Unilateral collapsed lung= central obstructive
lesion (bronchogenic CA, endobronchial tumor, FB), pneumonectomy,
unilateral
lung agenesis/hypoplasia, pulmonary artery atresia/hypoplasia
4.
Focal tracheal stricture=Extrinsic
compression (PA sling with napkin-ring tracheal rings), prolonged
intubation
scarring, endobronchial TB (multiple stenosis), amyloidosis (does not
spare
post membrane), wegner’s, CA
5.
Finger-in-glove=CF, ABPA
(asthma), bronchial atresia, central malignancy with distal plugging
6.
Unilateral hyperlucent lung
a.
Don’t miss: PTX, PE (ologemia), FB
(RLL>LLL)
b.
CLE (LUL>RML>RUL), bronchial atresia
c.
Bronchiolitis Obliterans (Swyer james in kids
<8yo)
d.
Poland’s, unilat mastectomy, large bulla
(emphysema)
>>MEDIASTINUM
1.
Lymph
nodes stations (IASLC
2009)
a.
1=supraclavicular (low cervical)
b.
2R/L=upper paratracheal
c.
3A/P A=prevascular (ant mediastinal and ant to left brachicephalic vein); P=prevertebral (retrotracheal)
d.
4R/L=lower paratracheal
e.
5=subaortic (AP window)
f.
6=para-aortic (phrenic)
g.
7=subcarinal
h.
8=para-esophageal (below carina)
i.
9=pulm ligament
j.
10R/L=hilar
k.
11R/L=interlobar
l.
12/13/14R/L=lobar/segmental/subsegmental
(peribronchial)
2.
Mediastinal
lesions
a.
Ant med mass
i.
Thymus
1.
Thymic hyperplasia (rebound s/p chemo/xrt
>50% increase in vol above baseline; Myasthenia gravis=85%
hyperplasia and
15% thymoma)
2.
Thymic cyst (unilocular/multilocular; may have
peripheral calc)
3.
Thymolipoma (b9, soft tumor that drapes down
and may change shape w/ decub)
4.
Thymoma (middle age pts;
b9=encapsulating with homogenous enhancing
capsule, may have lobulated contours and can be cystic VS
invasive=malignant with irreg margins, invasion/encasement of
mediastinal fat
and may have drop mets into pleura or pericardial involvement; assoc
with MG=40%
w/ thymoma have MG and 10-15% with MG have thymoma; can be cystic w/
mural
nodule; 5% may have calcs)
5.
Thymic CA (no capsule; can be metastatic--assoc
w/ mediastinal lymphadenopathy which is uncommon with thymoma; poor
prognosis)
ii.
Teratoma
and other germ cell tumors (<20yo; mature/immature/malig)
iii.
Terrible
lymphoma (homogenous mass which encases vessels; HD vs NHL)
iv.
Thyroid
substernal goiter
v.
Mets
(neuroblastoma)
vi.
Fibrosing
mediastinitis (TB, histo)
vii.
Mediastinal
lipomatosis (steroids, obese, cushing’s=endogenous steroids)
b.
Cystic med mass
i.
Duplication
(enteric/neuroenteric) vs bronchogenic cyst (subcarinal)
ii.
Pericardial
cyst (R>L)
iii.
Thymic
cyst (unilocular/multilocular; may have peripheral calc)
iv.
Cystic
thymoma (can have mural nodule)
v.
Teratoma (<20yo;
look for fat, fat-fluid level, calcification)
c.
Fatty med mass
i.
Epicardial
fat pad
ii.
Mediastinal
lipomatosis
iii.
Thymolipoma
iv.
Teratoma
v.
Hernia (morgagni
usually on the right; omental fat)
d.
Calcified med mass
i.
Fibrosing
mediastinitis (TB, histo; SVC syndrome, pulm HTN)
ii.
Treated
lymphoma
iii.
Teratoma
(<20yo; contains fat)
iv.
Thyroid
substernal goiter
v.
Calcified
nodes= TB , sarcoid/silicosis (egg-shell calcs)
e.
Cardiophrenic angle mass
i.
Epicardial
fat pad
ii.
Pericardial
cyst
iii.
Duplication
cyst
iv.
Thymolipoma
v.
Epiphrenic
LN
vi.
Hernia
f.
Paraspinal mass
i.
Neuroenteric
cyst (w/ vertebral anomaly)
ii.
Neurogenic
tumor (schwannoma, NF, paraganglioma, neuroblastoma)
iii.
Extramedullary
hematopoiesis
iv.
Duplication
or bronchogenic cyst
v.
Descending
aortic aneurysm
3.
Vascular
anomalies
a.
Bovine arch
b.
Double arch (R arch is larger/higher/posterior
than L with midline trachea and descending left aorta; encircles
trachea and
eso in a tight complete ring)
c.
Right arch
i.
Higher
assoc with truncus but TOF overall more common
ii.
2 types:
mirror image(worse b/c assoc cardiac anomalies like truncus or TOF) vs R arch
with aberrant LS
iii.
Can be
complete ring if intact lig arteriosus or open PDA
d.
Aberrant subclavian (travels post to eso)
i.
L arch
with aberrant R subclavian (dysphagia lusoria; diverticulum Kommerell)
ii.
R arch
with aberrant L subclavian
e.
Pulmonary sling (LPA arising from RPA; travels
btwn trachea and eso; retrotracheal density more caudal than aberrant
subclavian; napkin-ring tracheal rings)
f.
Cervical arch
g.
Anomalous vessel lateral to aortic arch
i.
PAPVR
ii.
Persistent
left SVC (left common cardinal vein starts near jct of SC and IJ,
descends
lateral to aortic arch and anterior to left hilum, courses post wall of
LA, and
dumps into coronary sinus)
h.
Enlarged azygous vein (note:
azygous of rightàin
SVC;
hemiazygous of leftàinfo
brachiocephalic vein)
i.
Azygous continuation
of IVC
ii.
CHF
iii.
TR
iv.
Constrictive
pericarditis
v.
SVC
obstruction distal to azygous entry
vi.
Portal HTN
i.
Heterotaxy syndrome
i.
Asplenia
ii.
Polysplenia
4.
Aorta
a.
Aneurysm
i.
Thoracic
aorta (ectasia 3.7-4.0cm, mild enlargement 4.0-4.5cm, ≥4.5cm aneurysm,
≥6cm
surgery)
1.
LVOT
2.
Aortic annulus
(at valve)
3.
Aortic root
(SOV)
a.
“Cusp to cusp”
measurement (cardiologists) upto 4cm
b.
Mean “cusp to
commisure” (preferred)
4.
Sinotubular
jct (STJ)
5.
Asc aorta
(@MPA) upto 3.7cm
6.
Aortic arch
7.
Aortic isthmus
(btwn take off of left subclavian artery and ductus arteriosus)
8.
Prox desc
aorta (@MPA)
9.
Distal desc
aorta (@dia hiatus) upto 2.8cm
ii.
Ectasia vs
true aneurysm (fusiform vs saccular)
iii.
Sinus of
valsalva aneurysm >4cm
iv.
Annuloaortic
ectasia (tulip bulp; Marfans or ED)
v.
Post-stenotic
dilation secondary to aortic stenosis
vi.
Syphilis
aortitis (calcifications)
vii.
Mycotic
aneurysm (saccular with surrounding inflammation)
viii.
Ductus bump or diverticula (anteromedial;
gentle obtuse bulge as opposed to sharp acute margins of pesudoaneurysm)
ix.
Traumatic
pseudoaneurysm (acute margins with aorta; saccular without atheroma; at
aortic
isthmus; s/ trauma)
x.
Infundibulum
of aortic arch/branch vessels
b.
Intra-mural hematoma (within aortic wall;
hyperdense crescent on non-contrast CT; better prognosis if
<2cm; treat it
like focal dissection)
c.
Mural thrombus (within aneurysm) vs
eccentric/ concentric intraluminal thrombus
d.
Penetrating aortic ulcer (PAU; thru existing
atheroma and projecting beyond aortic wall)
e.
Ulcerative plaque (does not project beyond
aortic wall)
f.
Dissection
i.
Stanford
A=asc aorta (60%); Stanford B=begins beyond brachiocephalic vessels
(40%)
ii.
CXR:
widened mediastinum, double or irreg aortic contour, inward
displacement of
athero calcs
iii.
Intimal
flap
1.
True lumen (smaller b/c compressed by false lumen;
surrounded by intimal calcification; brighter lumen)
2.
False lumen (larger b/c higher pressure; beak
sign=wedges around true lumen; cobweb sign=linear media remnants; lower
contrast density if patent due to delayed opacification; may be
completely/partially thrombosed or contain thrombus)
iv.
Complications
1.
Aortic rupture
2.
Coronary artery occlusion (acute MI usually
involves RCA)
3.
Aortic valve incompetence (acute aortic
insufficiency)
4.
Rupture into pericardial sac with cardiac
tamponade
5.
Extension into arch/branch vessels with or
without occlusion
a.
End-organ perfusion compromise
b.
Ischemic stroke
c.
Limb ischemia
d.
Paraplegia (artery of adamkiewicz to anterior
spinal artery)
v.
Chronic
dissection flap (thicker, straighter and may be calcified)
vi.
Intramural
hematoma is a variant
vii.
Acute
aortic injury
1.
CXR: widened mediastinum, indistinct/irreg
aortic contour, deviation of trachea to right, depression of LMSB, left
apical
pleural cap, thickened paraspinal stripe
2.
Location: isthmus (most common; located btwn
left subclavian artery and lig arteriosus)>asc aorta=desc aorta
at dia
hiatus
3.
Findings: irreg aortic contour with mural
hematoma; laceration/transection with active extravasation of contrast;
pseudoaneurysm; peri-aortic/mediastinal hematoma (+/-
pericardial/pleural
hematoma); focal intimal flap/clot; look for concomitant left
subclavian artery
injury
4.
Ddx=ductus bump or diverticula
5.
Cardiac
i.
LAE=
oblique measurement from LA border (double density) to mid point of
LMSB
>7cm on PA view; slayed carina >90-100deg; walking man
sign of
posteriorly displaced LMSB on lateral view
ii.
LVE=Hoffman
rigler sign (LV extends more than 1.8cm beyond posterior border of IVC
at 2cm
cephalad from intersection of LV and IVC on “true” lateral)
iii.
RAE=not
well discernable on CXR
iv.
RVE=upper
tipped “boot-shaped” apex; filling of retrosternal clear space;
enlarged MPA
v.
Acute
MR=RUL edema
vi.
Sig
PS=left PA enlargement
vii.
Sig AS=asc
aorta enlargement (look for valvular calcifications)
viii.
LV aneurysm
1.
True=post-MI; wide neck; may contain thrombus;
usually inferolateral wall
2.
False=post-trauma (aka pseudoaneurysm); narrow
neck; may rupture; usually posterolateral wall; less common
ix.
Cardiac
mass
1.
Thrombus (bland vs tumor)
2.
Metastasis (esp ACC, HCC, RCC, Hepatoblastoma
and Wilm’s)—10-20x more common than primary cardiac tumor
3.
Primary cardiac tumor
a.
B9=myxoma (LA>RA), rhabdomyoma (kids w/
TS); hemangioma (T2 bright); fibroma (kids)
b.
Malig=angiosarcoma (#1), rhabdosarcoma (#2)
x.
Pericardial
effusion= infection
(TB, viral), uremia, CVD (SLE, RA), mets,
post-MI/post-pericardiotomy (dressler’s syndrome usually after2wks—also
assoc
with pleural effusion and parenchymal opacities)
6.
Chest
wall/pleura
a.
Rib lesion= “FAME”
fibrous dysplasia, ABC, mets/myeloma, EG,
enchondroma
b.
Chest wall mass=
hematoma, primary or met bone tumors (consider askin’s, ewing’s, EG,
neuroblastoma in kids; don’t forget chondrosarcoma) hematoma, fibrous dysplasia,
schwannoma/NF,
fibrosarcoma/MFH, OM, elastofibroma dorsi
c.
Pleural mass or encasement= empyema
(split pleura sign), loculated effusion, fibrothorax (TB),
mesothelioma, mets
(breast/melanoma), lymphoma, invasive thymoma (co-exiting ant med
mass),
fibrous tumor of pleura (focal)
d.
Pleural calcifications= asbestos
exposure, old hemothorax/empyema, fibrothorax (TB)
e.
PTX=asthma/COPD,
trauma, EG/LAM, sarcoma
mets, catamenial, , barotrauma, spontaneous
7.
LUNG
CA
(stage IIIB is unresectable)
a.
Incidence:
AdenoCA>SCC>BAC>Small cell
(AFIP)
b.
Prognosis: SCC>Large
cell>BAC>AdenoCA>Small cell
c.
Small Cell
i.
Smokers
ii.
Unresectable
iii.
Paraneoplastic
syndromes (hypercalcemia, cushing, SIADH) with oat cell subtypes
iv.
Centrally
located (extensive LAD may result in SVC syndrome)
v.
Staging:
“limited dz” (confined to tolerable radiation port incld
supraclavicular node,
regional mediastinal, or effusion) vs “extensive dz”
d.
Non-small cell
i.
AdenoCA
1.
Non-smoker women
2.
Peripherally located
3.
Subtype=BAC, scar carcinoma
ii.
SCC
(epidermoid)
1.
Smokers
2.
Centrally located (around airways but not
within it unlike small cell)
3.
May cavitate
4.
Dysplasiaàin-situàSCC
5.
Good prognosis (b/c slow growing)
6.
Subtype=pancoast (superios sulcus tumor) w/
SVC syndrome, horner’s, brachial plexopathy, dysphagia
iii.
Large cell
1.
Rapid growth
2.
Peripherally located
e.
Staging
i.
Size (2cm,
2.1-3cm, 3.1-5cm, 5.1-7cm)
1.
Size>7cm (T3)
ii.
Location
iii.
Multicentric
tumor (synchronous) of same histology
1.
Satellite nodule in same lobe (T3)
2.
Nodule(s) in different ipsilateral lobe (T4)
3.
Contralateral lung nodule(s) i.e.
intrathoracic met (M1a)
iv.
Aggressive
features
1.
Direct visceral pleural
invasion (T2)
2.
Direct parietal pleural
invasion aka
chest wall (including superior sulcus tumors), diaphragm, phrenic
nerve,
mediastinal pleura, and/or parietal pericardium (T3)
3.
Invasion of mediastinum, heart, great vessels,
carina, trachea, eso, vertebral body, recurrent laryngeal nerve (T4)
v.
Endobronchial
lesion
1.
Endobronchial lesion not proximal to lobar
bronchus (T1)
2.
Endobronchial lesion ≥2cm from carina or
complete atelectasis/post-obstr pneumonitis extending to hilum but not
involving entire lung (T2)
3.
Endobronchial lesion <2cm from carina or
partial atelectasis/post-obstr pneumonitis involving entire lung (T3)
4.
Endobronchial lesion with involvement of
carina (T4)
vi.
Nodal
involvement
1.
N1=ipsilateral hilar or peribronchial
2.
N2=ipsilateral mediastinal and subcarinal
3.
N3=contralateral hilar/mediastinal;
supraclavicular; scalene
vii.
Malignant
effusion i.e. pleural dissemination or pleural nodules (not direct
pleural
invasion) and/or Malignant pericardial effusion (M1a)
viii.
Distant (extrathoracic) met (M1b)
>>HRCT
a.
History
and Labs
i.
Age
(20-40yo=sarcoid, EG, CVD; consider IPF in >50yo)
ii.
Sex
(LAM exclusively in women)
iii.
Smoking
hx (smokers=EG, RB/RBILD/DIP; non-smokers=HP, sarcoidosis)
iv.
Time
course (acute onset=AIP)
v.
Family
hx (LAM, sarcoidosis)
vi.
Exposure/toxins
(pets/hobbies/occupation/home environment)
vii.
CVD
(RA, scleroderma etc)
viii.
Malignancy
ix.
Symptoms
(no extrapulm sxs in IPF; CP pleurisy in CVD)
x.
Labs
(PFTS with DLCO, ANA, RF, ANCA, anti-BM ab, cryoglobulins,
hypersensitivity
panel)
b.
Location/distribution
i.
Focal
vs patchy vs diffuse
ii.
Upper,
middle, lower lobe pre-dominant (vs panlobar)
iii.
Peripheral
vs central vs peribronchovascular (sarcoid,
lymphangitic spread, LIP,
lymphoma or lymphoproliferative d/o, amyloid)
iv.
Reticular,
reticulonodular, micronodular
v.
What
is “fibrosis”? intra-lobular septal thickening (fine reticulation),
traction
bronchiectasis, honeycombing all are considered fibrosis
c.
Lines
i.
Peripheral
reticular pattern if
lower lobe
predominant
1.
UIP
2.
Fibrotic
NSIP assoc with chronic CVD (esp
scleroderma) and RA (distal clav absorption)
3.
Drug
toxicity (BAM=bleomycin, amiodarone,
methotrexate)
4.
Asbestosis
(parenchymal bands and curvilinear
subpleural lines)
5.
Chronic
emphysema (smoking-related interstitial
dz)
ii.
linear
pattern (aka lines radiating from hila +/- kerley lines)
“LIFE”
1.
Lymphagitic
spread
2.
(Atypical)
infection like viral/mycoplasma
3.
Fibrosis
like IPF
4.
Edema
iii.
Septal
thickening
1.
Intra-lobular
(fine reticular=fibrosis)
2.
Inter-lobular
septal thickening (secondary
lobules)—if not the predominant finding, can ignore this!!
a.
Smooth
septal thickening (water=edema,
pus=infx, blood=hemorrhage, protein=PAP)
b.
Nodular
septal thickening (sarcoid,
lymphangitic spread, LIP, lymphoma or lymphoproliferative d/o, amyloid)
c.
Irregular
(any fibrosing lung dz)
iv.
Subpleural
lines or parenchymal bands (scarring/fibrosis, atelectasis,
asbestosis)
d.
Nodules
i.
Micronodules
(<3-5mm)
1.
Centrilobular
(evenly spaced, don’t extend to
pleura or fissure)
a.
GG
(ill-defined)
i.
HP
subacute in non-smoker (classic), hemosiderosis
ii.
RB
or RBILD in smokers (“subtle GG nodules” in smokers)
iii.
Associated
with NSIP (CVD) and OP/COP
b.
Solid
with TIB (90% infectious
bronchiolitis)
i.
Think
inflammatory /infectious bronchiolitis vs Aspiration
1.
STAB=
smokers, TB/MAI, Aspiration,
Bronchiolitis, BAC (endobronchial adenoCA), BronchoPNA (patchy
clustered
nodules)
ii.
If
central mucus plugging (finger-in-glove), consider asthma, CF, ABPA
iii.
Mimicker=tumor
emboli (branching tumor in enlarged vessel in peribronchovascular
distribution)
iv.
AIDS-related
airways disease
v.
Endobronchial
mucinous adenoCA (BAC)
c.
Solid
without TIB
i.
Pneumoconiosis/Silicosis
(look for PMF etc)
ii.
EG
(aka pulm LCH)--if nodules are dense; may cavitate
2.
Perilymphatic
(patchy and abut pleura and
fissure)
a.
Sarcoid,
lymphangitic spread, LIP, lymphoma or
lymphoproliferative d/o, amyloid
3.
Random
(aka miliary; diffuse/uniform unlike perilymphatic)
a.
METS-B=hematogenous
mets (thyroid/renal/melanoma),
EG, miliary TB/fungal/disseminated viral, sarcoid/silicosis, BAC
ii.
Branching
nodules within enlarged vessel in peribronchovascular distribution =
consider
tumor emboli
e.
GGO
(can see vessels thru it)
i.
Differential
similar to consolidation
ii.
“ABCDEH”=
PAP, BOOP/COP, PCP,
DIP, Drugs, Edema,
HP, Hemorrhage
iii.
Acute vs chronic
1.
Acute
GGO
a.
Edema
(CHF and in ICU pts consider ARDS/DAD/AIP)
b.
Hemorrhage
(hemosiderosis)
c.
Atypical
infx (PCP in AIDS and CMV in
post-transplant)
d.
Subacute
HP (“head-cheese”)
2.
Chronic
GGO
a.
PAP
(“crazy paving”=geographic GG with septal
thickening), PCP (UL cysts and perihilar GG in HIV pt)
b.
BOOP/COP
(peribronchial and subpleural “polygonal”
fleeting consolidations, GGO, and nodules)
c.
DIP
and NSIP
d.
Drugs
(BAM=bleomycin, amiodarone, methotrexate)
e.
HP
(exposure)
f.
BAC
iv.
Crazy
paving ddx= PAP, pulm edema, pulm hemorrhage, PNA
(bacterial), BAC
v.
History
helps
1.
Hemoptysis=hemorrhage
2.
Immunocompromised=infx
(PCP)
3.
Exposure=HP
(non-smoker)
4.
CVD
or ILD=alveolitis
f.
Mosaic
attenuation
i.
How
to tell from GGO=Geographic (sharply demarcation on inspiratory view),
differential vessel size (smaller in lucent areas), air-trapping (on
expiration
dark areas remain dark), stable over time
ii.
Note:
Mosaic attenuation is an INSPIRATORY HRCT finding while air-trapping is
a
EXPIRATORY HRCT findings!!
iii.
small
airways disease vs small vessel disease à
do expiratory view to distinguish btwn the two
iv.
SMALL
VESSEL DISEASE (less common) =no air-trapping; larger areas
of non-lobular
lucencies with normal vessel size; pulm HTN and R heart enlargement
1.
Chronic
PE (look for associated pulm HTN)
2.
Vasculitis
(CVD)
v.
SMALL
AIRWAYS DISEASE =with air-trapping; lobular areas of
lucencies with small
vessel size; peribronchial thickening;
1.
Direct
signs of small airways dz=bronchial wall
thickening, bronchiolectasis, centrilobular nodules with TIB
2.
Indirect
signs of small airways disease dz=
mosaic attenuation (described in inspiration), air-trapping (described
in
expiration; mosaic attenuation persists and contours get even more
sharply
marginated)
3.
Bronchiolitis
a.
Smokers
(RB, RBILD)
b.
Infectious
(viral in kids like
RSV/adenovirus/mycoplasma; MAC/TB/fungal in adults)
i.
Swyer
James (recurrent viral infx in kids <8yo; unilateral hyperlucent
small lung
identified on CXR)
c.
Diffuse
panbronchiolitis (exclusively Japanese)
d.
Follicular
bronchiolitis (CVD like sjogrens, RA,
HIV)
4.
B.O./constrictive
bronchiolitis (swyer
james in kids <8yo with unilat hyperlucent small lung identified
on CXR)
a.
Etiology:
i.
Recurrent
viral infx
ii.
Toxic
fume exposure (smoking, NO2 silo worker, SO2, popcorn worker diacetyl)
iii.
Drugs
like penicillamine
iv.
CVD,
RA
v.
Chronic
transplant rejection (after lung transplant or GVHD after BM transplant)
b.
Features
i.
Hyperlucent
lobe/lung on inspiration
ii.
Bronchial
dilation and peribronchial thickening (due to constriction of distal
bronchioles)
iii.
Air-trapping
only seen upon
expiration (mosaic
attenuation)
5.
Bronchitis
vi.
MOSAIC
ATTENUATION without centrilobular nodules or TIB
1.
Smokers
2.
Asthma/chronic bronchitis
3.
HP
4.
Follicular
bronchiolitis
5.
B.O.
g.
Consolidation
or airspace disease
i.
Diffuse
airspace dz (*=acute)
1.
*water=CHF/ARDS
(STD=shock, sepsis, trauma,
drugs like crack cocaine)
2.
*pus=PNA
3.
*blood=hemorrhage
(wegners, goodpasture,
hemosiderosis)
4.
cells=lymphoma/BAC/OP
5.
fat=lipoid
PNA
6.
protein=PAP
ii.
Upper-lobe
predominant= “CASSET-P” cystic fibrosis, ank spond,
sarcoidosis/silicosis,
EG, TB, PCP
iii.
Peripheral
consolidation= “AEIOU” alveolar sarcoid, chronic Eos PNA,
infarct, OP/COP,
UIP
iv.
Migratory/fleeting
infiltrates= ABC acute eos PNA, ABPA, Aspiration, BOOP/COP,
Chugg Straus
(kids)
v.
Dense
consolidations= amiadarone, talcosis (IV drug abuse), PMF
(sarcoid/silicosis), amyloidosis, asbestos plaques (mimicker on CXR)
vi.
Chronic
infiltrates= BALLS BAC/lymphoma, Alveolar sarcoid, lipoid
PNA/PAP,
sequestration, chronic eos PNA
vii.
Interstitial
infiltrate=LIFE lymphangitic spread (adenoCA), infx
(viral/atypical PNA),
fibrosis (IPF), edema
viii.
Infiltrate
in kids= round PNA, plasma
cell granuloma, CCAM, CLE, CDH, sequestration, duplication cyst, mets
h.
Cysts/Cavitation
i.
Emphysema
(blebs vs bullae)
1.
Centrilobular
vs Panlobular (lower lobe
predominance; α-1-antitrypin def)
2.
Paraseptal
3.
Cicatricial
(assoc with scarring or PMF)
ii.
Cysts
1.
Blebs
(<1cm), bullae (>1cm), pneumatocele
2.
Cavitation
a.
Wall
thickness
i.
<4mm
(93% b9)
ii.
4-15mm
(50% b9 and 50% malignant)
iii.
>16
mm (99% malig)
b.
Inner
wall appearance
i.
Smooth
(non-specific)
ii.
Nodular=CA
iii.
Shaggy=infx
c.
DDX
cavitary lesions= “CT-SWAP” ca
(primary SCC or secondary SCC like H&N males and cervical
females),
TB/fungal, septic emboli (feeding vessel sign), wegners (sinusitis) /
RA
(necrobiotic), abscess, aspergillosis (GG halo), papillomatosis, others
(sarcoid, EG or PLCH, infarct), cystic bronchiectasis
d.
DDX
cystic lesion with increased lung volumes=
EG (male smokers >30yo), LAM (young females), CF, bullous
emphysema, cystic
bronchiectasis
e.
DDX
thick cavity cyst with debris= infx
(necrotizing PNA with pulm gangrene; TB/sarcoid/CF with mycetoma),
infarct, CA,
hydatid
f.
DDX
cystic lesion kid= CLE, CCAM (I/II),
CDH, bronchogenic cyst, pneumatocele, cavitary PNA/abscess/TB
iii.
Bronchiectasis
1.
Cylindrical
vs varicose (beaded) vs cystic
(saccular)
2.
Bronchiectasis
ddx
a.
Recurrent
infx/aspiration (like TB, MAI=lady
widemere)
b.
Finger-in-glove=CF/ABPA
c.
Congenital=immotile
cilia (kartageners)/william-campbell
(Mounier Kuhn=tracheobronchomegaly)
d.
Fibrosis=traction
bronchiectasis
e.
Emphysema
iv.
Honeycombing
1.
Associated
with interface sign=irreg margins of
pleural and vessels; associate with traction bronchiectasis (corkscrew)
2.
Honeycombing
ddx: “SCHARD”=sarcoidosis, CVD,
chronic HP, asbestosis, RA, drug toxicity
3.
Lower
lobe fibrosis= UIP or IPF, fibrotic
NSIP assoc with chronic CVD (esp scleroderma), drug toxicity
(“BAM”=bleomycin,
amiodarone, methotrexate), asbestosis (parenchymal bands and
curvilinear
subpleural lines), RA (distal clav absorption), chronic emphysema
4.
End-stage
lung dz= UIP, CVD (esp
scleroderma), sarcoid, chronic HP, asbestosis, RA
i.
Others
i.
Air-trapping
(emphysema, BO/swyer james, LAM, EG, CF)
ii.
LN
(not uncommon in IPF esp if <15mm and only involves 1-2 nodal
stations like
paratracheal or subcarinal; usually responds to therapy like steroids)
1.
Low
density LAD= TB/MAI, wipples/crohns,
untreated lymphoma, mets (testicular etc)
2.
High
density LAD= castlemans, carcinoid,
Kaposi, LN mets from RCC (hemorrhage)
3.
Calcified
LAD= TB, sarcoid/silicosis, treated
lymphoma, papillary thyroid CA
iii.
Effusion
(pleural/pericardial)—think CVD or RA
iv.
HIV
“please test my CDfour”
1.
CD4>200:
candida/Kaposi/TB (secomdary)
2.
CD4<200:
PCP, TB (primary)
3.
CD4<100:
Toxo
4.
CD4<75:
MAC
5.
CD4<50:
CMV/PMLE/Fungal
>>ILD
classification
i.
Acute
1.
Hemorrhage
2.
Infx
(viral, mycoplasma)
3.
Drug
rxn
4.
Edema
ii.
Chronic
1.
ILD
2.
Inhalational
(HP, asbestosis, silicosis)
3.
Smoking-related
(emphysema)
4.
Lymphangitic
spread
5.
CVD
(including RA, sarcoidosis)
b.
Chronic
fibrosing IP
i.
UIP (IPF)
1.
Age
>50-70yo M>F
2.
More
common in smokers or ex-smokers (may have
emphysema in upper lobes)
3.
Patchy,
bilateral peripheral/subpleural
reticulations and honeycombing (with or without traction bronchiectasis)
4.
Basal-predominant
5.
Calcification
within areas of fibrosis =
dendriform pulmonary ossifications
6.
Some
GG opacities but not the major feature
(biopsy should be directed here)
7.
Poor
prognosis
8.
“accelerated deterioration
of UIP” if acutely
worsening SOB and develop sig GG opacities
9.
5-10%
develop lung CA (can hide in peripheral
areas of honeycombing esp in lower lobes)
10.
“possible UIP” (absent
honeycombing) and
“inconsistent with UIP” àrequires
biopsy
11.
If
patient has known underlying process like RA, asbestosis, or CVD like
scleroderma—don’t call it UIP!!! (instead call it chronic rheumatoid
lung)
12.
Pirfenidone
and Nintedanib (slows progression and improves survival)
13.
Honeycombing
ddx: “SCHARD”=sarcoidosis, CVD, chronic HP, asbestosis, RA, drug
toxicity
ii.
NSIP
1.
More
common in females (younger pts ~40-50yo)
2.
Not
associated with smoking 70% (usually associated
with CVD)
3.
Cellular
(better; pred GGO) vs fibrotic (GGO +
retculations) vs mixed
4.
Lower
lobe GG opacities with intra-lobular
septal thickening (diffuse and confluent, not just peripheral like UIP)
5.
Classic
“subpleural sparing” dorsally
6.
Lower
lobe volume loss
7.
Usually
no honeycombing (but may have traction
bronchiectasis)
8.
Search
for etiology like CVD, drug-induced,
environmental exposure like HP (otherwise, idiopathic)
9.
Acute
exacerbation uncommon
10.
Some
improve with tx while some remain stable for years (only minority
progress to
honeycombing aka progress to UIP)
c.
Smoking-related
IP
(some of these may co-exist)
i.
RB (asymptomatic)
1.
Asymptomatic
smokers
2.
“Subtle”
GG centrilobular nodules (more subtle
than HP)
3.
Minimal
GG
(aka dirty lung)
4.
Peribronchial
thickening
5.
+/-
air-trapping emphysema
ii.
RB-ILD (=RB + symptoms)
1.
Symptomatic
heavy smokers (>30pack-years;
40-50yo)
2.
Findings
of RB with more extensive GG opacities
3.
Peribronchial
thickening
4.
Air-trapping
(emphysema)
5.
Self-limiting
iii.
DIP (not very common; less common than
RBILD)
1.
M>F
smokers (30-40yo)
2.
Bibasilar
predominance GG with +/-fine
reticulations (not much septal thickening)
3.
Classic
“cystic changes within GG opacities”ßmay
represent bleb
related to emphysema
4.
No
fibrosis
5.
Treat
with cessation of smoking and steroids
iv.
EG (pulmonary LCH)
1.
20-40yo
smokers, M+F, whites more common
2.
Upper
lobe pred nodules à thin-walled cyst à
thick-walled cyst à
irregular/bizzare-shaped cysts
3.
25%
develop PTX
4.
10%
develop extrapulm findings
5.
Part
of Histiocytosis X: PLCH (adults),
Letterer-Siwe (kids), Hand-Schuller-Christian (kids)
v.
Pulmonary fibrosis related to smoking
1.
Upper
lobe honeycombing, septal thickening, and
traction bronchiectasis
vi.
CPFE (combined pulmonary fibrosis &
emphysema)
1.
60-70yo
male who are heavy smokers
2.
Upper
lobe emphysema
3.
Lower
lobe NSIP fibrosis
4.
Lung
vol are preserved
5.
Decreased
DLCO
6.
50%
have pulm HTN
7.
Worse
prognosis than UIP
d.
Acute/subacute
IP
i.
OP/COP
1.
More
common in non-smokers
2.
Assoc
with infx, drugs, autoimmune dz (esp
myositis syndromes)
3.
Acute
onset <3mos of flu-like syndrome (SOB/cough/fever/chills/wtloss)
4.
Peribronchial
and subpleural consolidations (“polygonal
shaped” or irregular)—can be migratory (may have lobar predominance,
not
diffuse)
5.
GGO
(crazy paving)
6.
Centrilobular
nodules
7.
Classic
“reverse halo” or “atoll” sign (rare but
specific)
8.
Involve
mid to lower lung
9.
May
have small effusion
10.
Can
be idiopathic or assoc with CVD, drugs, aspiration, infx
11.
Restrictive
lung disease like other ILDs
12.
Excellent
response to steroids (with complete recover in most pts)
13.
Main
DDx is chronic eos PNA can look very similar (look for peripheral eso)!!
ii.
DAD/AIP (Hamman rich)
1.
AIP=
idiopathic ARDS (which responds to steroids
which are generally avoided in infectious ARDS)—if have patient with
ARDS who
is not responding to conventional tx, consider this diagnosis
2.
Acute
(<1wk) fulminant (ICU
patients)
3.
Appearance
similar to ARDS but higher mortality
4.
Diffuse
confluent GG sparing CPAàproliferative/organizingà
anterior upper lobe
fibrosis fibrotic with traction bronchiectasis
e.
Others
entities
i.
LIP
1.
B9
lymphoproliferative disorder with lymphocytic
infiltrates
2.
Exclusively
in Sjogrens or RA (adults) or AIDS
(kids<13yo)
3.
Retriculonodular
pattern, GGO, and cysts
a.
Peribronchovascular
and centrilobular nodules
b.
GGO
c.
Peribronchovascular/subpleural/randomly-distributed
cysts
4.
Associated
with monoclonal or polyclonal
gammopathy
5.
May
progress to lymphoma (5%)
ii.
HP (EAA)
1.
Organic
antigen=EAA (farmer, bird fancier,
pigeon breeder etc)
2.
Inorganic
antigen=pneumoconiosis
3.
Acute
(lower lobe pred; diffuse airspace dz w/
GGO; mimics edema or ARDS)=symptoms <1mo
4.
Subacute
(symptoms wks to 4mos)
a.
Upper
to mid lung
b.
GG
Centrilobular nodules (classic—ddx is
hemosiderosis or RBILD if subtle)
c.
Head-cheese
(mosaic attenuation)
5.
Chronic
(fibrosis in similar pattern as the
head-cheese pattern of subacute dz with mosaic attenuation and
air-trapping)=symptoms >4mos to yrs
6.
Smoking
is protective (tell the pigeon-fancier
to start smoking!)
iii.
PPFE (pleuroparenchymal fibroelastosis)
1.
50-60yo
(usually post-lung or BM transplant)
2.
Similar
to fibrotic TB in upper lung zone
3.
Peripheral
upper lobe fibrosis, pleural
thickening, and upward retraction of hila
f.
CVD
(usually associated with NSIP)
i.
RA (constrictive bronhiolitis and BOOP may co-exist)
1.
Pleural/pericardial
effusion
2.
Necrobiotic
nodules
3.
Distal
clavicular erosions
ii.
Scleroderma
1.
Dilated
eso
2.
Pulm
HTN
3.
Calcinosis
(calc arounds joints if CREST
syndrome)
iii.
SLE
(lupus)
1.
Fibrosis
uncommon
2.
Pleural/pericardial
effusion
3.
Pulm
HTN
iv.
Sjogrens
1.
Rare
to have IPF
2.
LIP
v.
DM/PM
1.
Soft
tissue calcifications in DM
|
